Division of Kidney Diseases and Hypertension, Department of Internal Medicine, Hofstra-North Shore-LIJ School of Medicine, Hofstra University, Great Neck, NY 11021, USA.
Ren Fail. 2012;34(2):251-3. doi: 10.3109/0886022X.2011.647210. Epub 2012 Jan 23.
We report a case of a renal transplant patient who was maintained on tacrolimus and diltiazem therapy and developed tacrolimus toxicity leading to reversible acute kidney injury when started on ranolazine. A 62-year-old Caucasian male status post renal transplant in 2009 (on prednisone and tacrolimus) was evaluated for ischemic heart disease and was initiated on ranolazine 500 mg tablets twice daily, which was later increased to 1000 mg twice daily. After 2 weeks, he developed fatigue, loss of appetite, tremors, and decreased urine output and was admitted to our hospital. His other significant medications included enalapril 2.5 mg and diltiazem 240 mg daily. The patient was awake and alert, but lethargic. He was found to be bradycardic with a heart rate of 42/min. The rest of his physical examination was benign. His electrocardiogram revealed sinus bradycardia. Laboratory studies revealed serum creatinine of 2.4 mg/dL from a baseline of 1.5 mg/dL (stable for the past 2 years). The tacrolimus trough was elevated at 14 ng/mL, which decreased after stopping ranolazine, reaching 7 ng/mL after 3 days, while continuing the same dose of tacrolimus. His creatinine trended downward and reached his baseline of 1.5 mg/dL over the next 2 days. His bradycardia and other symptoms resolved after cessation of ranolazine. He was discharged to follow up, to initiate an alternate agent for ischemic heart disease. Specific pharmacokinetic studies are warranted to study these drug interactions, and tacrolimus levels should be closely monitored in transplant patients who initiate ranolazine treatment.
我们报告了一例肾移植患者的病例，该患者接受他克莫司和地尔硫卓治疗，在开始使用雷诺嗪时发生他克莫司毒性导致可逆性急性肾损伤。一名 62 岁白人男性，2009 年接受肾移植（泼尼松和他克莫司），因缺血性心脏病接受评估，并开始服用雷诺嗪 500mg 片剂，每日两次，后来增加到每日两次 1000mg。2 周后，他出现疲劳、食欲不振、震颤和尿量减少，并被收入我院。他的其他重要药物包括依那普利 2.5mg 和地尔硫卓 240mg，每日一次。患者意识清醒警觉，但嗜睡。他被发现心动过缓，心率为 42/min。他的其他体检均正常。他的心电图显示窦性心动过缓。实验室研究显示血清肌酐从基线的 1.5mg/dL 升高至 2.4mg/dL（过去 2 年稳定）。他克莫司谷值升高至 14ng/mL，停用雷诺嗪后降至 7ng/mL，同时继续使用相同剂量的他克莫司。他的肌酐呈下降趋势，在接下来的 2 天内降至基线 1.5mg/dL。停用雷诺嗪后，他的心动过缓及其他症状得到缓解。他出院随访，为缺血性心脏病启动替代药物。需要进行特定的药代动力学研究来研究这些药物相互作用，并且在开始使用雷诺嗪治疗的移植患者中应密切监测他克莫司水平。
